Abstract: :
Purpose: Following retinal ischemia/reperfusion in the rat,retinal ganglion cell (RGC) degeneration occurs due to neurotoxicityof glutamate and nitric oxide (NO) generated by inducible nitricoxide synthese (NOS-2). We have previously presented that treatmentwith aminoguanidine significantly reduced the loss of RGCs followingischemia. However, several recent reports suggest that reactiveoxygen species (ROS) play an important role of neurodegenerationas well. We have studied whether ROS caused the loss of RGCsfollowing ischemia/reperfusion injury.Methods: Retinal ischemiawas produced by transient elevation of intraocular pressureabove systolic blood pressure for 75 minutes by intraocularcannulation. MCI-186, an radical scavenger, was injected intravenouslytwo times of 3mg/kg, during ischemia and 30minutes after ischemiaas group I for determining early phase of neurodegeneration,4 and 5 days after ischemia as group II for determining latephase of neurodegeneretion and saline injected group as control.Loss of RGCs was determined quantitatively by retrograde labelingwith Fluoro-Gold.Results: One week after ischemia, untreatedanimals lost 28.4±1.7% [mean±SD] RGCs centrallyand 38.5±3.9% RGCs peripherally (n=4). Treatment withMCI-186 significantly reduced the loss of RGCs following ischemia21.3±3.3% centrally (P=0.0339) and 31.4±2.7% peripherally(p=0.0339) in group I (n=3), however no significant differencein the both central (28.2±3.2%, p>0.9999) and peripheral(38.1±3.1%, p=0.5959) part of retina in the group II(n=3).Conclusions: Our results demonstrate that MCI-186 hasneuroprotective effect in retinal ischemia/reperfusion in therat. ROS play a part of role of early phase of RGCs degenerationfollowing ischemia/reperfusion injury.